I. Field of the Invention
The present invention relates generally to the field of cardiac rhythm management devices, including atrial, ventricular, and dual chamber pacemakers. More specifically, the present invention relates to a cardiac pacing system that improves the ability to automatically detect whether a pacing stimulus results in heart capture or contraction. The cardiac pacing system includes a pacing/sensing circuit that attenuates polarization voltages or “afterpotentials” which develop at the heart tissue/electrode interface following the delivery of a stimulus to the heart tissue. The pacing/sensing circuit of the present invention may utilize the pacing electrodes to sense a response evoked by the pacing stimulus. Thus, the present invention allows accurate detection of an evoked response of the heart, to thereby determine whether each pacing stimulus results in capture.
II. Discussion of the Prior Art
Cardiac pacers have enjoyed widespread use and popularity through time as a means for supplanting some or all of an abnormal heart's natural pacing functions. The various heart abnormalities remedied by pacemakers include total or partial heart block, arrhythmias, myocardial infarctions, congestive heart failure, congenital heart disorders, and various other rhythm disturbances within the heart. The general components of a cardiac pacemaker include an electronic pulse generator for generating stimulus pulses to the heart coupled to an electrode lead arrangement (unipolar or bipolar) positioned adjacent or within a preselected heart chamber for delivering pacing stimulus pulses.
Regardless of the type of cardiac pacemaker employed to restore the heart's natural rhythm (ie: ventricular pacing, atrial pacing, or dual chamber pacing in both the atrium and ventricle), each type operates to stimulate excitable heart tissue cells adjacent to the electrode of the pacing lead employed with the pacemaker, which may or may not result in capture. Myocardial response to stimulation or “capture” is a function of the positive and negative charges found in each myocardial cell within the heart. More specifically, the selective permeability of each myocardial cell works to retain potassium and exclude sodium such that, when the cell is at rest, the concentration of sodium ions outside of the cell membrane is significantly greater than the concentration of sodium ions inside the cell membrane, while the concentration of potassium ions outside the cell membrane is significantly less than the concentration of potassium ions inside the cell membrane. The selective permeability of each myocardial cell also retains other negative particles within the cell membrane such that the inside of the cell membrane is negatively charged with respect to the outside when the cell is at rest. When a stimulus is applied to the cell membrane, the selective permeability of the cell membrane is disturbed and it can no longer block the inflow of sodium ions from outside the cell membrane. The inflow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as depolarization, causes the myocardial cell to have a net positive charge due to the inflow of sodium ions. The electrical depolarization of the cell interior causes a mechanical contraction or shortening of the myofibril of the cell. The syncytial structure of the myocardium will cause the depolarization originating in any one cell to radiate through the entire mass of the heart muscle so that all cells are stimulated for effective pumping. Following heart contraction or systole, the selective permeability of the cell membrane returns and sodium is pumped out until the cell is re-polarized with a negative charge within the cell membrane. This causes the cell membrane to relax and return to the fully extended state, referred to as diastole.
In a normal heart, the sino-atrial (SA) node initiates the myocardial stimulation of the atrium. The SA node comprises a bundle of unique cells disposed within the roof of the right atrium. Each cell membrane of the SA node has a characteristic tendency to leak ions gradually over time such that the cell membrane periodically breaks down and allows an inflow of sodium ions, thereby causing the SA node cells to depolarize. The SA node cells are in communication with the surrounding atrial muscle cells such that the depolarization of the SA node cells causes the adjacent atrial muscle cells to depolarize. This results in atrial systole wherein the atria contract to empty blood into the ventricles. The atrial depolarization from the SA node is detected by the atrioventricular (AV) node which, in turn, communicates the depolarization impulse into the ventricles via the Bundle of His and Purkinje fibers following a brief conduction delay. In this fashion, ventricular systole lags behind atrial systole such that the blood from the ventricles pumps through the body and lungs after being filled by the atria. Atrial and ventricular diastole follow wherein the myocardium is re-polarized and the heart muscle relaxed in preparation for the next cardiac cycle. It is when this system fails or functions abnormally that a cardiac pacer may be needed to deliver an electronic pacing stimulus for selectively depolarizing the myocardium of the heart so as to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
The success of a pacing stimulus in depolarizing or “capturing” the selected chamber of the heart hinges on whether the current of the pacing stimulus as delivered to the myocardium exceeds a threshold value. This threshold value, referred to as the capture threshold, is related to the electrical field intensity required to alter the permeability of the myocardial cells to thereby initiate cell depolarization. If the local electrical field associated with the pacing stimulus does not exceed the capture threshold, then the permeability of the myocardial cells will not be altered enough and thus no depolarization will result. If, on the other hand, the local electrical field associated with the pacing stimulus exceeds the capture threshold, then the permeability of the myocardial cells will be altered sufficiently such that depolarization will result.
Changes in the capture threshold may be detected by monitoring the efficacy of stimulating pulses at a given energy level. If capture does not occur at a particular stimulation energy level which previously was adequate to effect capture, then it can be surmised that the capture threshold has increased and that the stimulation energy should be increased. On the other hand, if capture occurs consistently at a particular stimulation energy level over a relatively large number of successive stimulation cycles, then it is possible that the capture threshold has decreased such that the stimulation energy is being delivered at level higher than necessary to effect capture.
The ability of a pacemaker to detect capture is desirable in that delivering stimulation pulses having energy far in excess of the patient's capture threshold is wasteful of the pacemaker's limited power supply. In order to minimize current drain on the power supply, it is desirable to automatically adjust the pacemaker such that the amount of stimulation energy delivered to the myocardium is maintained at the lowest level that will reliably capture the heart. To accomplish this, a process known as “capture verification” must be performed wherein the pacemaker monitors to determine whether an evoked depolarization occurs in the preselected heart chamber following the delivery of each pacing stimulus pulse to the preselected chamber of the heart.
The conventional pacemaker typically includes a pacing output circuit designed to selectively generate and deliver stimulus pulses through a lead to one or more electrodes positioned in the heart of a patient. The pacing output circuit includes a power supply, switches, a pacing charge storage capacitor, and a coupling capacitor, all of which cooperatively operate under the direction of a controller to perform a charging cycle, a pacing cycle, and a recharging cycle. The capacitance of the pacing charge storage capacitor typically ranges between 10–30 microfarads so as to develop a sufficient pacing charge for stimulating the heart. The capacitance of the coupling capacitor typically ranges between 15 to 40 microfarads with 33 microfarads being typical. A capacitor having a capacitance in this range was believed necessary to deliver sufficient energy to the heart.
The charging cycle involves manipulation of the switches such that the pacing charge storage capacitor is charged up to a predetermined voltage level. The pacing cycle involves manipulating the switches such that the voltage within the pacing charge storage capacitor may be discharged through the coupling capacitor to the electrodes of the pacemaker. The recharging cycle involves further manipulation of the switches for a predetermined period of time following the pacing pulse to allow the coupling capacitor to be discharged.
While the conventional pacing circuit is generally effective in delivering stimulus pulses to a selected chamber of the heart, it has been found that the detection of evoked depolarization or “capture verification” is rendered very difficult due to polarization voltages or “afterpotential” which develop at the heart tissue/electrode interface following the application of the stimulation pulses. The ability to verify capture is further affected by other variables including patient activity, body position, drugs being used, lead movement, noise etc.
In the past, the large capacitance of coupling capacitor was believed necessary in order to sufficiently block any DC components from the heart and to minimize pace pulse voltage droop. However, the large capacitance of the coupling capacitor causes a charge dissipation or “afterpotential” which is relatively large (100 mV or greater) and which decays exponentially over a relatively long period of time (100 milliseconds). This is particularly troublesome due to the fact that the evoked potential of the heart tissue is small in amplitude relative to the polarization voltage or “afterpotential” (100 mV). The amplitude of the evoked potential corresponding to a P-wave typically ranges between 1–5 mV and the amplitude of the evoked potential corresponding to an R-wave typically ranges between 5–20 mV.
Further, the long decay period of the polarization voltage or “afterpotential” effectively masks the evoked potential, which typically begins within approximately (10–40) milliseconds after the stimulation pulse to a selected chamber of the heart. It will be appreciated that this creates difficulty in detecting the evoked response of the heart following the delivery of stimulus pulses. In that evoked response is indicative of capture, the undesirable masking of the evoked response by “afterpotential” thus hampers the ability of the pacemaker to conduct automatic capture verification. Hence, there is a need for a cardiac pacing system that decreases and/or shortens the pacing afterpotential with minimal increase of the leading edge voltage pacing threshold. It is also desirable to reduce the number or complexity of the implanted components and, thus, there is a need for a pacing system having a pacing/sensing circuit that minimizes the number of required electrodes positioned within the heart for sensing a response evoked by a pacing stimulus directed to a preselected chamber of the heart.
Sholder in U.S. Pat. No. 5,222,483 recognizes that sensing a signal for verification of capture is extremely difficult because of the saturation voltage present following the generation of a stimulation pulse, which makes it difficult to accurately detect the voltage representing P-waves while discriminating against other signals present in the atrium. Sholder describes a capture verification circuit that requires an indifferent electrode disposed on the front or back of the connector top of the pacemaker or alternatively positioned on an additional lead or added to one of the pacing leads. The capture sensing lead and/or indifferent electrode required by Sholder increases the complexity and required components of the pacing system and may increase the cost thereof.
Hence, there is a need for a cardiac pacing system that attenuates polarization voltages or “afterpotentials” which develop at the heart tissue/electrode interface following the delivery of a stimulus to the heart tissue, and which minimizes the number of required components of the cardiac pacing system. The present invention meets these needs.